Updates on NF-kappaB

Posted on 15. March 2009 by Vince Giuliano

The nuclear transcription factor NF-kappaB plays a prominent role in one of the advanced theories of aging, Programmed genetic changes.  Several new pieces of research highlight the mechanisms by means of which this multi-faceted substance impacts on aging and the importance of the anti-aging firewall substances that inhibit the expression of NF-kappaB.  I mention two such studies.

One study has to do with the role of Tumor Necrosis Factor (TNF) activating the expression of NF-kappaB in Muscle Progenitor Cells (MPC).  This study is also relevant to the fourteenth theory of aging, Decline in adult stem cell differentiation.  TNF acts via a number of pathways in a complicated manner including activation of NF-kappaB to produce a variety of effects including induction of apoptosis (cell suicide).  This apoptosis is useful when cancers are concerned but is also potentially destructive of healthy cells. It appears that in MPC cells at least, TNF-alpha activates NF-κappaB more in older animals than in younger ones.  This leads to apoptotic signaling and death of MPC.  The problem is thought to be a decline in age of effective cellular mechanisms for keeping NF-kappaB inactive.  Practically speaking, this appears to support the importance of the thirty-nine anti-aging firewall substances that inhibit the expression of NF-kappaB.

A second study has to do with the role of the sirtuin SIRT6 in regulating the expression of NF-kappaB.  Another member of the sirtuin family, SIRT1, has been extensively studied and even sometimes referred to as a key “longevity gene.” But SIRT6 also seems to play an important role in keeping NF-kappaB expression in its proper place.  SIRT6 works with NFkappa-B to control the activity of genes connected with metabolism, inflammation, immunity and aging. When SIRT6 is in short supply, NFkappa-B becomes hyperactive and turns up activity of aging-linked genes.  “We propose that SIRT6 attenuates NF-kappaB signaling via H3K9 deacetylation at chromatin, and hyperactive NF-kappaB signaling may contribute to premature and normal aging.”  Again, taking the firewall substances that control expression of NFkappa-B may be an effective anti-aging measure.

About Vince Giuliano

Being a follower, connoisseur, and interpreter of longevity research is my latest career. I have been at this part-time for well over a decade, and in 2007 this became my mainline activity. In earlier reincarnations of my career. I was founding dean of a graduate school and a university professor at the State University of New York, a senior consultant working in a variety of fields at Arthur D. Little, Inc., Chief Scientist and C00 of Mirror Systems, a software company, and an international Internet consultant. I got off the ground with one of the earliest PhD's from Harvard in a field later to become known as computer science. Because there was no academic field of computer science at the time, to get through I had to qualify myself in hard sciences, so my studies focused heavily on quantum physics. In various ways I contributed to the Computer Revolution starting in the 1950s and the Internet Revolution starting in the late 1980s. I am now engaged in doing the same for The Longevity Revolution. I have published something like 200 books and papers as well as over 430 substantive.entries in this blog, and have enjoyed various periods of notoriety. If you do a Google search on Vincent E. Giuliano, most if not all of the entries on the first few pages that come up will be ones relating to me. I have a general writings site at www.vincegiuliano.com and an extensive site of my art at www.giulianoart.com. Please note that I have recently changed my mailbox to vegiuliano@agingsciences.com.
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